FURTHER EVIDENCE FOR THE MITOGENIC ACTION OF URINARY TRYPSIN-INHIBITOR

We have previously shown that urinary trypsin inhibitor (UTI), also kn own as bikunin, was mitogenic for human fibroblasts at low concentrati ons, and growth-inhibitory at higher concentrations, and have identifi ed high- and low-affinity cellular binding sites for this protein. We have now investigated fibroblast proteins which interact with bikunin. Bikunin binds to proteins of about 50K and 250K. The simplest interpr etation is that the 50K protein may be a proteinase which is also the low-affinity bikunin binding site, involved in growth inhibition, and that the larger protein mag; be responsible for the mitogenic response to bikunin. Inhibitors of intracellular calcium mobilisation also inh ibit the mitogenic response to bikunin, and, by the measurement of the efflux of pre-loaded Ca-45(2+), bikunin at mitogenic concentrations c an be shown to stimulate calcium mobilisation.